Evidence map›Paper›PMID 27096033›Full record

ReviewWorld journal of gastrointestinal oncology2016

Targeting inflammation in pancreatic cancer: Clinical translation.

Colin William Steele, Nina Angharad Kaur Gill, Nigel Balfour Jamieson, Christopher Ross Carter

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastrointestinal oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. A Humanized Patient-Derived Xenograft Model for Pancreatic Cancer.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
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  10. p110γ deficiency protects against pancreatic carcinogenesis yet predisposes to diet-induced hepatotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  11. Review
  12. Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Colin William SteeleColin William Steele, Nigel Balfour Jamieson, Christopher Ross Carter, Department of Pancreaticobiliary Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom.
Nina Angharad Kaur GillColin William Steele, Nigel Balfour Jamieson, Christopher Ross Carter, Department of Pancreaticobiliary Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom.
Nigel Balfour JamiesonColin William Steele, Nigel Balfour Jamieson, Christopher Ross Carter, Department of Pancreaticobiliary Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom.
Christopher Ross CarterColin William Steele, Nigel Balfour Jamieson, Christopher Ross Carter, Department of Pancreaticobiliary Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom.
Creative Research Enterprises (United States) · USGlasgow Royal Infirmary · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preclinical modelling studies are beginning to aid development of therapies targeted against key regulators of pancreatic cancer progression. Pancreatic cancer is an aggressive, stromally-rich tumor, from which few people survive. Within the tumor microenvironment cellular and extracellular components exist, shielding tumor cells from immune cell clearance, and chemotherapy, enhancing progression of the disease. The cellular component of this microenvironment consists mainly of stellate cells and inflammatory cells. New findings suggest that manipulation of the cellular component of the tumor microenvironment is possible to promote immune cell killing of tumor cells. Here we explore possible immunogenic therapeutic strategies. Additionally extracellular stromal elements play a key role in protecting tumor cells from chemotherapies targeted at the pancreas. We describe the experimental findings and the pitfalls associated with translation of stromally targeted therapies to clinical trial. Finally, we discuss the key inflammatory signal transducers activated subsequent to driver mutations in oncogenic Kras in pancreatic cancer. We present the preclinical findings that have led to successful early trials of STAT3 inhibitors in pancreatic adenocarcinoma.

Indexed as

InflammationMicroenvironmentPancreatic cancerStroma

Identifiers

PMID27096033
PMCPMC4824716
OpenAlexW2467828327

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.